Gene interactions and pathways from curated databases and text-mining

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ABL1 — EPHB2

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: ABL1 → EPHB2 (decreases, EPHB2 Activity, ABL1 Activity) Yu et al., Oncogene 2001*
    Evidence: Interestingly, treatment of COS cells and B35 neuronal-like cells with ephrin-B1 to activate endogenous EphB2 decreased the kinase activity of endogenous Abl.
  • KEGG Axon guidance: EPHB1/EPHB2/EPHB3/EPHB4/EPHB6 → ABL1 (protein-protein, activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Renshaw et al., Oncogene 2000 (MAP Kinase Signaling System) : Expression of a kinase-defective c-Abl specifically inhibited the transient induction of Erk2 activity following cell adhesion
Yu et al., Oncogene 2001 : Activated EphB2 causes tyrosine phosphorylation of Abl and Arg, and vice versa
Li et al., EMBO J 2001 (MAP Kinase Signaling System) : In vivo expression of a Grb2 mutant where Tyr209 was changed to phenylalanine enhanced BCR/ABL induced ERK activation and fibroblast transformation, and potentiated and prolonged Grb2 mediated activation of Ras, mitogen activated protein kinase and c-Jun N-terminal kinase in response to EGF stimulation
Wilson et al., Oncogene 2002 (Cell Transformation, Neoplastic...) : These data implicate the Src kinase family in Stat5 and Erk activation downstream of Bcr-Abl , and identify myeloid-specific Src kinases as potential drug targets in CML
Baughn et al., J Virol 2005 (Cell Transformation, Viral) : Expression of DN Shc reduced Ab-MLV pre-B-cell transformation and decreased the ability of v-Abl to stimulate Ras activation and Erk phosphorylation in a Raf dependent but Rac independent fashion
Sirvent et al., Oncogene 2007 (Breast Neoplasms...) : Moreover, Abl mediates Src induced extracellular regulated kinase 5 (ERK5) activation to drive cell transformation
Aceves-Luquero et al., PloS one 2009 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : In fact, Bcr/Abl activates preferentially Erk2 in transient transfection in a dose dependent fashion through the c-Abl part of the chimeric protein
Liu et al., Int J Cardiol 2011 (Carotid Artery Injuries...) : In vivo, ABL ( 26 mg/kg/day ) significantly suppressed injury induced ERK1/2 phosphorylation, and increased VSMC apoptosis 14 days after balloon injury
Lu et al., Cell cycle (Georgetown, Tex.) 2010 : Here we show that Abl is necessary for p38alpha/beta activation initiated by N-cadherin ligation, but in contrast to Cdo, Abl is also required for N-cadherin dependent ERK activation
Jia et al., Am J Physiol Cell Physiol 2012 (MAP Kinase Signaling System) : Abl regulates smooth muscle cell proliferation by modulating actin dynamics and ERK1/2 activation ... The results suggest that Abl may regulate smooth muscle cell proliferation by modulating actin dynamics and ERK1/2 phosphorylation during mitogenic activation
Mokhtari et al., Diabetologia 2013 : Imatinib stimulated ERK ( thr202/tyr204 ) phosphorylation in a c-Abl dependent manner
Tanaka et al., Mol Cell Biol 1995 : These results suggest that both Crk and Grb2 may contribute to the activation of Erk by oncogenic Abl , whereas Nck is unlikely to participate in this pathway